1. Field of the Invention
This invention relates to a novel technique for the treatment of spinal cord injuries in mammals.
2. Description of the Prior Art
In U.S. Pat. Nos. 3,853,993 and 3,788,468, it is disclosed that certain water-soluble carotenoids had been observed to possess quite unique properties. In particular, these water-soluble carotenoids have been found to increase the diffusivity of oxygen through aqueous media. The effect was found further to be useful biologically in the treatment of atherosclerosis, which had been theorized as being a disease resulting from local hypoxia of the vascular walls.
The study of the biological effects of this compound had continued with the discovery that it is also effective in the treatment of cerebral edema (U.S. patent application filed concurrently herewith).
It has now been found that the water soluble carotenoids are quite effective in the treatment of spinal cord injuries.
Spinal cord injury is a condition characterized by contusion of the neural tissue with resultant decrease or loss of its ability to function properly and transmit nerve impulses. The usual cause is due to an impact injury of some nature, but it may also occur during the manipulation attendant to certain surgical procedures. The early changes which occur are hemorrhagic and ischemic lesions which appear in central portions (gray matter) of the spinal cord. Initially, the periphery of the cord will show only occasional small hemorrhages in the usual case. With time the white matter in the periphery of the spinal cord will develop progressive edema, leading eventually to necrosis of this area.
The initial loss of central gray matter can be tolerated by man and most animals, since the resultant neurologic deficit is not great. However, with white matter loss in the periphery of the cord, the distal functioning fibers and neurons are rendered useless. And, with a segmental loss of white matter paraplegia or quadriplegia occurs.
The edema and necrosis in the white matter has a temporal separation of perhaps a few hours from the time of injury. Obviously then any therapeutic modality which would prevent these changes from occurring would be of great benefit in the treatment of these injuries and in the attenuation of paralysis resulting from them. At the present time no satisfactory treatment has been devised for this condition.
A number of investigators in recent years have demonstrated that the sequential pathologic changes following spinal cord injury involve alterations of vascular dynamics and progressive ischemia. The edema and necrosis which follow have been considered to be secondary changes, resulting from ischemia. Experimentally, certain modalities of therapy which have involved providing a relative increase in available oxygen have been shown to be of benefit. Hyperbaric oxygenation was studied by Kelly, DL Jr., Lassiter, KRL, Vongsvivut, A, Smith, JM: Effects of hyperbaric oxygenation and tissue oxygen studies in experimental paraplegia. J. Neurosurg. 36:425-429, 1972 and shown to be beneficial. Hypothermia by means of localized spinal cord cooling has been effective in various studies. By this method, a decrease in cellular metabolic needs would result in a decreased oxygen need. Dexamethasone has heretofor been shown to improve the functional result: Black, P. Markowitz, RA: Experimental spinal cord injury in monkeys: comparison of steroids and local hypothermia. Surg Forum. 22:409-411, 1971.
The reason why dexamethasone is effective for this purpose however, has never been clearly understood. It was believed that this compound had some effect in altering the permeability of certain tissues in the vicinity of the injury through which fluids could be passed.